Archive for the ‘Addictions and Habits’ Category

ScienceDaily (July 12, 2012) — Adverse childhood experiences (ACEs) can stay with us for life. New research published in BioMed Central’s open access journal Substance Abuse Treatment, Prevention, and Policy explains how these events can be tied up with adult smoking patterns, especially for women, and suggests that treatment and strategies to stop smoking need to take into account the psychological effects of childhood trauma.

ACEs can range from emotional, physical, and sexual abuse to neglect and household dysfunction and affect a large range of people. In one of the largest studies of ACEs survey over 60% of adults reported a history of at least one event. ACEs are thought to have a long term effect on the development of children and can lead to unhealthy coping behaviour later in life.

Since psychiatric disorders, including depression and anxiety, are known to increase the risk of smoking, researchers across the USA collaborated to investigate the effects of psychological distress on the relationship between ACE and current adult smoking. The ACE questionnaire was completed by over 7000 people, about half of whom were women.

Even after adjusting the data for factors known to affect a person’s propensity for smoking, such as their parents smoking during the subject’s childhood, and whether or not they had drunk alcohol in the previous month), women who had been physically or emotionally abused were 1.4 times more likely to smoke. Having had a parent in prison during childhood doubled chances of women smoking.

Psychological distress increases the chances that any person (male or female) will smoke. Dr Tara Strine, who led this study commented, “Since ACEs increase the risk of psychological distress for both men and women, it seemed intuitive that an individual experiencing an ACE will be more likely to be a tobacco cigarette smoker. However, in our study, ACEs only to increased the risk of smoking among women. Given this, men who have experienced childhood trauma may have different coping mechanisms than their female counterparts.”

Dr Strine continued, “Our results show that, among women, an underlying mechanism that links ACEs to adult smoking is psychological distress, particularly among those who have suffered emotional or physical abuse or physical neglect as a child. These findings suggest that current smoking cessation campaigns and strategies may benefit from understanding the potential relationship between childhood trauma and subsequent psychological distress on the role of smoking particularly in women.”

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ScienceDaily (July 11, 2012) — A change in the formula of the frequently abused prescription painkiller OxyContin has many abusers switching to a drug that is potentially more dangerous, according to researchers at Washington University School of Medicine in St. Louis.

The formula change makes inhaling or injecting the opioid drug more difficult, so many users are switching to heroin, the scientists report in the July 12 issue of the New England Journal of Medicine.

For nearly three years, the investigators have been collecting information from patients entering treatment for drug abuse. More than 2,500 patients from 150 treatment centers in 39 states have answered survey questions about their drug use with a particular focus on the reformulation of OxyContin.

The widely prescribed pain-killing drug originally was thought to be part of the solution to the abuse of opioid drugs because OxyContin was designed to be released into the system slowly, thus not contributing to an immediate “high.” But drug abusers could evade the slow-release mechanism by crushing the pills and inhaling the powder, or by dissolving the pills in water and injecting the solution, getting an immediate rush as large amounts of oxycodone entered the system all at once.

In addition, because OxyContin was designed to be a slow-release form of the generic oxycodone, the pills contained large amounts of the drug, making it even more attractive to abusers. Standard oxycodone tablets contained smaller amounts of the drug and did not produce as big a rush when inhaled or injected.

Then in 2010, a new formulation of the drug was introduced. The new pills were much more difficult to crush and dissolved more slowly. The idea, according to principal investigator Theodore J. Cicero, PhD, was to make the drug less attractive to illicit users who wanted to experience an immediate high.

“Our data show that OxyContin use by inhalation or intravenous administration has dropped significantly since that abuse-deterrent formulation came onto the market,” says Cicero, a professor of neuropharmacology in psychiatry. “In that sense, the new formulation was very successful.”

The researchers still are analyzing data, but Cicero says they wanted to make their findings public as quickly as possible. The new report appears as a letter to the editor in the journal. Although he found that many users stopped using OxyContin, they didn’t stop using drugs.

“The most unexpected, and probably detrimental, effect of the abuse-deterrent formulation was that it contributed to a huge surge in the use of heroin, which is like OxyContin in that it also is inhaled or injected,” he says. “We’re now seeing reports from across the country of large quantities of heroin appearing in suburbs and rural areas. Unable to use OxyContin easily, which was a very popular drug in suburban and rural areas, drug abusers who prefer snorting or IV drug administration now have shifted either to more potent opioids, if they can find them, or to heroin.”

Since the researchers started gathering data from patients admitted to drug treatment centers, the number of users who selected OxyContin as their primary drug of abuse has decreased from 35.6 percent of respondents before the release of the abuse-deterrent formulation to 12.8 percent now.

When users answered a question about which opioid they used to get high “in the past 30 days at least once,” OxyContin fell from 47.4 percent of respondents to 30 percent. During the same time period, reported use of heroin nearly doubled.

In addition to answering a confidential questionnaire when admitted to a drug treatment program, more than 125 of the study subjects also agreed to longer phone interviews during which they discussed their drug use and the impact of the new OxyContin formulation on their individual choices.

“When we asked if they had stopped using OxyContin, the normal response was ‘yes,'” Cicero says. “And then when we asked about what drug they were using now, most said something like: ‘Because of the decreased availability of OxyContin, I switched to heroin.'”

These findings may explain why so many law enforcement officials around the country are reporting increases in heroin use, Cicero says. He compares attempts to limit illicit drug use to a levee holding back floodwaters. Where the new formulation of OxyContin may have made it harder for abusers to use that particular drug, the “water” of illicit drug use simply has sought out other weak spots in the “levee” of drug policy.

“This trend toward increases in heroin use is important enough that we want to get the word out to physicians, regulatory officials and the public, so they can be aware of what’s happening,” he says. “Heroin is a very dangerous drug, and dealers always ‘cut’ the drug with something, with the result that some users will overdose. As users switch to heroin, overdoses may become more common.”

Funding for this research comes from the Denver Health and Hospital Authority, which provided an unrestricted research grant to fund the Survey of Key Informants’ Patients (SKIP) Program, a component of the RADARS (Researched Abuse, Diversion and Addition-Related Surveillance) System.

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ScienceDaily (July 10, 2012) — Moderate consumption of alcohol is associated with a reduced risk of developing rheumatoid arthritis, suggests a study published on the British Medical Journalwebsite.

The results show that women who regularly consume more than three alcoholic drinks a week for at least 10 years have about half the risk of developing rheumatoid arthritis compared with non-drinkers.

After adjusting for factors such as age, smoking and dietary habits, women who reported drinking more than three glasses of alcohol per week in both 1987 and 1997 had a 52% reduced risk of rheumatoid arthritis compared with never drinkers at both assessments.

These findings add to a growing body of evidence that long term moderate alcohol consumption is not harmful and may protect against a chronic disease like rheumatoid arthritis, say the authors. However, they stress that the effect of higher doses of alcohol on the risk of rheumatoid arthritis remains unknown.

Rheumatoid arthritis is a chronic inflammatory joint disorder that usually develops between the ages of 40 and 50. About 1% of the world’s population is affected — women three times more often than men. Some studies have shown that drinking alcohol is associated with a lower risk of rheumatoid arthritis, whereas others have found no association.

The relation between alcohol intake and rheumatoid arthritis remains controversial. So a team of researchers based in Sweden set out to analyse this association among 34,141 Swedish women born between 1914 and 1948.

Detailed information about alcohol consumption, diet, smoking history, physical activity and education level was collected in 1987 and again in 1997.

Participants were followed up for seven years (Jan 2003 to Dec 2009) when they were aged 54-89 years, during which time 197 new cases of rheumatoid arthritis were registered.

The age-standardized rate of rheumatoid arthritis was smaller among women who drank more than four glasses of alcohol a week (7 per 10,000 person years) than among women who drank less than one glass a week (9.1 per 10,000 person years) as reported in 1997.

After adjusting for factors such as age, smoking and dietary habits, women who reported drinking more than three glasses of alcohol per week in both 1987 and 1997 had a 52% reduced risk of rheumatoid arthritis compared with never drinkers at both assessments.

One standard glass of alcohol was defined as approximately 500 ml beer, 150 ml of wine or 50 ml of liquor.

The reduced risk was similar for all three types of alcoholic drink.

Further analyses made little difference to the results, supporting the theory that a moderate amount of alcohol may be a protective factor for rheumatoid arthritis. The authors suggest that this is most likely to be due to alcohol’s ability to lower the body’s immune response.

This is relevant because rheumatoid arthritis is an autoimmune disease — it causes the immune system, which usually fights infection, to attack the cells that line the joints.

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ScienceDaily (Mar. 8, 2012) — Several decades ago, a number of clinics used LSD to treat alcoholism with some success. But until now, no research has pulled together the results of these trials to document exactly how effective LSD was. Now a new meta-analysis of randomized controlled trials of the drug, available in the Journal of Psychopharmacology, published by SAGE, provides evidence for a clear and consistent beneficial effect of LSD for treating alcohol dependency.

Teri Krebs and Pål-Ørjan Johansen are both affiliated with the Department of Neuroscience at the Norwegian University of Science and Technology (NTNU), Trondheim, Norway. During research fellowships at Harvard Medical School, Boston, USA, they spotted a gap in the understanding of lysergic acid diethylamide’s (LSD’s) potential for alcoholism treatment. No researcher had ever performed a quantitative meta-analysis of previous clinical trials using the drug.

Krebs and Johansen set out to independently extract data from previous randomized, controlled clinical trials, pooling their results. They identified six eligible trials, all carried out in the late 1960s and early 1970s. These included 536 participants, the vast majority of whom were male in-patients enrolled in alcohol-focused treatment programs. Individuals with a history of schizophrenia or psychosis were excluded from the original trials. The control conditions included low-dose LSD, stimulants, or non-drug control conditions. Each trial used clearly defined treatment-independent and standardized methods to assess outcomes on alcohol misuse.

While the experiments varied in the dosage used and the type of placebo physicians administered to patients, LSD had a beneficial effect on alcohol misuse in every trial. On average, 59 percent of LSD patients and 38 percent of control patients were improved at follow-up using standardized assessment of problem alcohol use. There was also a similar beneficial effect on maintained abstinence from alcohol. The positive effects of a single LSD dose — reported both in these and in other, non-randomized trials — lasts at least six months and appears to fade by 12 months.

Regarding the lasting effects of the LSD experience in alcoholics, investigators of one trial noted, “It was rather common for patients to claim significant insights into their problems, to feel that they had been given a new lease on life, and to make a strong resolution to discontinue their drinking.” And investigators of another trial noted, “It was not unusual for patients following their LSD experience to become much more self-accepting, to show greater openness and accessibility, and to adopt a more positive, optimistic view of their capacities to face future problems.”

LSD interacts with a specific type of serotonin receptors in the brain, which may stimulate to new connections and open the mind for new perspectives and possibilities, Krebs explains. LSD is not known to be addictive or toxic to the body, but the LSD has striking effects on imagination, perception, and memories and can elicit periods of intense anxiety and confusion.

“Given the evidence for a beneficial effect of LSD on alcoholism, it is puzzling why this treatment approach has been largely overlooked,” says Johansen. The authors suggest a number of reasons for this: many of the individual trials did not have enough patients to confidently conclude that there was a beneficial effect of LSD, but when pooled together the trials shows a clear and consistent effect; trial authors expected unrealistic results from a single dose of LSD and tended to discount moderate or short-term effects and; earlier non-randomized clinical trials reporting promising results but had methodological problems, creating the misunderstanding that well-designed studies did not exist or failed to find a beneficial effect. Finally, the complicated social and political history of LSD meant that obtaining regulatory approval for clinical trials became laborious, although national and international drug control measures have never banned treatment development or medical use of LSD.

Its unusual for a psychiatric medication to have a positive treatment effect lasting for several months after a single dose. Krebs and Johansen suggest that repeated doses of LSD coupled with modern, evidence-based alcohol relapse prevention treatments might provide more sustained results. They also note that plantbased psychedelics such as mescaline and ayahuasca which are used by Native Americans to promote mental health and sustained sobriety, merit further investigation for alcoholism treatment.

ScienceDaily (Mar. 8, 2012) — A single injection of cocaine or methamphetamine in mice caused their brains to put the brakes on neurons that generate sensations of pleasure, and these cellular changes lasted for at least a week, according to research by scientists at the Salk Institute for Biological Studies.

Their findings, reported March 7, 2012 in Neuron, suggest this powerful reaction to the drug assault may be a protective, anti-addiction response. The scientists theorize that it might be possible to mimic this response to treat addiction to these drugs and perhaps others, although more experiments are required to explore this possibility.

“It was stunning to discover that one exposure to these drugs could promote such a strong response that lasts well after the drug has left the body,” says Paul Slesinger, an associate professor in the Clayton Foundation Laboratories for Peptide Biology. “We believe this could be the brain’s immediate response to counteract the stimulation of these drugs.”

Scientists are trying to better understand the brain’s response to psychoactive drugs in hopes of finding new ways to prevent and treat addiction. This research has become especially important as the number of deaths due to drug abuse now exceeds those due to car accidents, with more than 37,000 people dying from drugs in 2009, according to the Centers for Disease Control and Prevention. Slesinger and Christian Lüscher, a long-time collaborator at the University of Geneva, have been investigating the cellular changes in the brain that occur with drug abuse.

Dopamine is a primary neurotransmitter used in the brain’s reward pathway — generally speaking, the activity of dopamine neurons in the reward pathway increases in response to rewards, such as sex, food and drugs. Psychostimulants, such as methamphetamine and cocaine, co-opt this pathway and alter the brain’s response to dopamine. Understanding the neuroadaptations that occur in the reward pathway in response to drugs of abuse may lead to the development of a treatment for drug addiction.

Previous research has shown that use of cocaine and methamphetamine in mice enhances excitatory connections to dopamine neurons. While most research has focused on these excitatory neurons, Slesinger and his colleagues looked at neurons that inhibit dopamine transmission, and found that one injection of cocaine or methamphetamine produces a profound change in the function of these inhibitory GABA neurons. These neurons were not able to control how they fired, so they would release more than the usual amount of inhibitory neurotransmitter.

“This persistent change in the inhibitory neurons occurs simultaneously with enhancement of excitatory inputs, indicating a possible compensatory mechanism that could be protective during exposure to drugs,” Slesinger says.

The Salk researchers identified a change in the biochemical pathway in inhibitory GABA neurons that led to this protective effect. It involved a change in the activity of a protein, known as a phosphatase, which controls the levels of a receptor known to be important for controlling the electrical activity of the GABA neuron.

“This particular pathway — involving a GABA type B receptor and a particular type of potassium channel — was affected by psychostimulants in these inhibitory neurons,” Slesinger says. “We noticed a dramatic reduction in the strength of this signaling pathway, which we showed was due to a decrease in the activity of the GABAB receptor and the potassium channel on the neuron’s membrane surface.”

“If we could tap into this pathway — enhance the ability of inhibitory neurons to control the activity of dopamine neurons — we might be able to treat some types of drug addiction,” Slesinger says.

What is not known is how long the drug response lasts — this study only looked at the brains of mice at two time points, 24 hours and seven days, after drug use — and why addiction ultimately develops with chronic drug use. These are questions Slesinger and his colleagues are now investigating.

The study’s two lead authors are Claire Padgett, a former postdoctoral researcher in the Slesinger laboratory, and Arnaud Lalive, a doctoral student at the University of Geneva, who is working in the laboratory of Christian Lüscher, also a co-author. Other participating investigators include: Michaelanne Munoz, of the University of California San Diego; Stephen Moss and colleagues from Tufts University School of Medicine; Rafael Luján, from the Universidad de Castilla-La Mancha in Albacete, Spain; and investigators from Hokkaido University School of Medicine in Sapporo, Japan; University College in London; and AstraZeneca in Cheshire, United Kingdom.

The study was funded by the National Institute on Drug Abuse, the National Institute of Neurological Disorders and Stroke, Catharina Foundation and the Spanish Ministry of Education and Science.

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ScienceDaily (July 3, 2012) — As the United States confronts the growing epidemic of obesity among children and adults, a team of University of Colorado School of Medicine obesity researchers concludes that what the nation needs is a new battle plan — one that replaces the emphasis on widespread food restriction and weight loss with an emphasis on helping people achieve “energy balance” at a healthy body weight.

In a paper published in the July 3 issue of the journal Circulation, James O. Hill, PhD. and colleagues at the Anschutz Health and Wellness Center take on the debate over whether excessive food intake or insufficient physical activity cause obesity, using the lens of energy balance — which combines food intake, energy expended through physical activity and energy (fat) storage — to advance the concept of a “regulated zone,” where the mechanisms by which the body establishes energy balance are managed to overcome the body’s natural defenses towards preserving existing body weight. This is accomplished by strategies that match food and beverage intake to a higher level of energy expenditure than is typical in America today, enabling the biological system that regulates body weight to work more effectively. Additional support for this concept comes from many studies showing that higher levels of physical activity are associated with low weight gain whereas comparatively low levels of activity are linked to high weight gain over time.

“A healthy body weight is best maintained with a higher level of physical activity than is typical today and with an energy intake that matches,” explained Hill, professor of pediatrics and medicine and executive director of the Anschutz Health and Wellness Center at the University of Colorado Anschutz Medical Campus and the lead author of the paper. “We are not going to reduce obesity by focusing only on reducing food intake. Without increasing physical activity in the population we are simply promoting unsustainable levels of food restriction. This strategy hasn’t worked so far and it is not likely to work in the future.

As Dr. Hill explains, “What we are really talking about is changing the message from ‘Eat Less, Move More” to ‘Move More, Eat Smarter.’ ”

The authors argue that preventing excessive weight gain is a more achievable goal than treating obesity once it is present. Here, the researchers stress that reducing calorie intake by 100 calories a day would prevent weight gain in 90 percent of the adult population and is achievable through small increases in physical activity and small changes in food intake.

People who have a low level of physical activity have trouble achieving energy balance because they must constantly use food restriction to match energy intake to a low level of energy expenditure. Constant food restriction is difficult to maintain long-term and when it cannot be maintained, the result is positive energy balance (when the calories consumed are greater than the calories expended) and an increase in body mass, of which 60 percent to 80 percent is usually body fat. The increasing body mass elevates energy expenditure and helps reestablish energy balance. In fact, the researchers speculate that becoming obese may be the only way to achieve energy balance when living a sedentary lifestyle in a food-abundant environment.

Using an exhaustive review of the energy balance literature as the basis, the researchers also refuted the popular theory that escalating obesity rates can be attributed exclusively to two factors — the change in the American diet and the rise in overall energy intake without a compensatory increase in energy expenditure. Using rough estimates of increases in food intake and decreases in physical activity from 1971 to 2000, the researchers calculated that were it not for the physiological processes that produce energy balance, American adults would have experienced a 30 to 80 fold increase in weight gain during that period, which demonstrates why it is not realistic to attribute obesity solely to caloric intake or physical activity levels. In fact, energy expenditure has dropped dramatically over the past century as our lives now require much less physical activity just to get through the day. The authors argue that this drop in energy expenditure was a necessary prerequisite for the current obesity problem, which necessitates adding a greater level of physical activity back into our modern lives.

“Addressing obesity requires attention to both food intake and physical activity, said co-author John Peters, PhD., assistant director of the Anschutz Health and Wellness Center. “Strategies that focus on either alone will not likely work.”

In addition, the researchers conclude that food restriction alone is not effective in reducing obesity, explaining that although caloric restriction produces weight loss, this process triggers hunger and the body’s natural defense to preserve existing body weight, which leads to a lower resting metabolic rate and notable changes in how the body burns calories. As a result, energy requirements after weight loss can be reduced from 170 to 250 calories for a 10 percent weight loss and from 325 to 480 calories for a 20 percent weight loss. These findings provide insight concerning weight loss plateau and the common occurrence of regaining weight after completing a weight loss regimen.

Recognizing that energy balance is a new concept for to the public, the researchers call for educational efforts and new information tools that will teach Americans about energy balance and how food and physical activity choices affect energy balance.

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ScienceDaily (July 2, 2012) — Researchers are closer to understanding the biology behind GHB, a transmitter substance in the brain, best known in its synthetic form as the illegal drug fantasy.

In the 1960s, gamma-hydroxybutyric acid (GHB) was first discovered as a naturally occurring substance in the brain. Since then it has been manufactured as a drug with a clinical application and has also developed a reputation as the illegal drug fantasy and as a date rape drug. Its physiological function is still unknown.

Now a team of researchers at the Department of Drug Design and Pharmacology at the University of Copenhagen has shown for the first time exactly where the transmitter substance binds in the brain under physiologically relevant conditions. The results have recently been published in the Proceedings of the National Academy of Sciences.

“We have discovered that GHB binds to a special protein in the brain — more specifically a GABAA-receptor. The binding is strong even at very low dosage. This suggests that we have found the natural receptor, which opens new and exciting research opportunities, in that we have identified an important unknown that can provide the basis for a full explanation of the biological significance of the transmitter,” says Laura Friis Eghorn, PhD student.

Illegal use and possible antidote

Fantasy is also used as a so-called date rape drug, because in moderate amounts it has sedative, sexually stimulating and soporific effects. The compound is also abused for its euphoric effect, but in combination with alcohol, for example, it is a deadly cocktail that can lead to a state of deep unconsciousness or coma.

“GHB is registered for use as a drug to treat alcoholism and certain types of sleep disorders, but the risk of abuse presents difficulties. In the long-term, understanding how GHB works will enable us to develop new and better pharmaceuticals with a targeted effect in the brain, without the dangerous side-effects of fantasy,” explains Laura Friis Eghorn, Department of Drug Design and Pharmacology.

Fantasy is an extremely toxic euphoriant, because the difference between a normal intoxicating dose and a fatal dose is so small. A better understanding of the biological mechanisms behind GHB-binding in the brain will benefit research into a life-saving antidote for this drug. Today there is no known antidote.

Statistics from Denmark in 2010 show that 8-10 percent of young people who frequent night clubs have had experience with Fantasy. However, since the drug is often also used in private for its sedative effect, it is difficult to estimate the extent of abuse.

Researchers on a targeted fishing expedition

The new research findings are the result of a collaboration between researchers at the University of Sydney in Australia and medicinal chemists at the Faculty of Health and Medical Sciences:

“Our chemist colleagues designed and produced special ligands — that are mimics of GHB in several variations. This enabled us to go on a targeted fishing expedition in the brain. We have slowly found our way to the receptor, which we have also been able to test pharmacologically. In itself, it is not unusual to find new receptors in the brain for known compounds. However, when we find a natural match rooted in the brain’s transmitter system, the biological implications are extremely interesting,” explains Petrine Wellendorph, associate professor and head of the responsible research group that produced the pioneering results.

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ScienceDaily (June 11, 2012) — Non-medical prescription drug use by college students is a growing trend on most campuses, according to the U.S. Department of Education’s Higher Education Center for Alcohol, Drug Abuse and Violence Prevention. Due to this trend, Western Illinois University Department of Health Sciences Assistant Professor Amanda Divin and her colleague, Keith Zullig, an associate professor in the West Virginia University School of Public Health, recently conducted and published a study that explores non-medical prescription drug use and depressive symptoms in college students.

Divin and Zullig utilized data from the fall 2008 American College Health Association National College Health Assessment (ACHA-NCHA), a national research survey that addresses seven areas of health and behavior of college students, one of which is alcohol, tobacco and other drug use. The sample used for the study (from the ACHA-NCHA data) contained 26,600 randomly selected college students from 40 campuses in the U.S. The student respondents were asked about their non-medical prescription drug use (including painkillers, stimulants, sedatives and antidepressants) and mental health symptoms within the last year.

According to Divin’s and Zullig’s results, approximately 13 percent of the college-student respondents reported non-medical prescription drug use, with those who reported feeling hopeless, sad, depressed or considered suicide being significantly more likely to report non-medical use of any prescription drug. The results also showed this relationship was more pronounced for females who reported painkiller use. The study — which is titled, “The association between non-medical prescription drug use, depressive symptoms, and suicidality among college students” — will appear in the August 2012 issue of Addictive Behaviors: An International Journal.

“Because prescription drugs are tested by the U.S. Food and Drug Administration and prescribed by a doctor, most people perceive them as ‘safe’ and don’t see the harm in sharing with friends or family if they have a few extra pills left over,” Divin explained. “Unfortunately, all drugs potentially have dangerous side effects. As our study demonstrates, use of prescription drugs — particularly painkillers like Vicodin and Oxycontin — is related to depressive symptoms and suicidal thoughts and behaviors in college students. This is why use of such drugs need to be monitored by a doctor and why mental health outreach on college campuses is particularly important.”

Divin and Zullig believe the results suggest that students are self-medicating their psychological distress with prescription medications.

“Considering how common prescription sharing is on college campuses and the prevalence of mental health issues during the college years, more investigation in this area is definitely warranted,” Divin added. “Our study is just one of the many first steps in exploring the relationship between non-medical prescription drug use and mental health.”

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ScienceDaily (June 5, 2012) — Mothers who use marijuana as teens — long before having children — may put their future children at a higher risk of drug abuse, new research suggests.

Researchers in the Neuroscience and Reproductive Biology section at the Cummings School of Veterinary Medicine conducted a study to determine the transgenerational effects of cannabinoid exposure in adolescent female rats. For three days, adolescent rats were administered the cannabinoid receptor agonist WIN-55, 212-2, a drug that has similar effects in the brain as THC, the active ingredient in marijuana. After this brief exposure, they remained untreated until being mated in adulthood.

The male offspring of the female rats were then measured against a control group for a preference between chambers that were paired with either saline or morphine. The rats with mothers who had adolescent exposure to WIN-55,212-2 were significantly more likely to opt for the morphine-paired chamber than those with mothers who abstained. The results suggest that these animals had an increased preference for opiate drugs.

The study was published in the Journal of Psychopharmocology and funded by the National Institutes of Health.

“Our main interest lies in determining whether substances commonly used during adolescence can induce behavioral and neurochemical changes that may then influence the development of future generations,” said Research Assistant Professor John J. Byrnes, the study’s lead author, “We acknowledge that we are using rodent models, which may not fully translate to the human condition. Nevertheless, the results suggest that maternal drug use, even prior to pregnancy, can impact future offspring.”

Byrnes added that much research is needed before a definitive connection is made between adolescent drug use and possible effects on future children.

The study builds on earlier findings by the Tufts group, most notably a study published last year in Behavioral Brain Research by Assistant Professor Elizabeth Byrnes that morphine use as adolescent rats induces changes similar to those observed in the present study.

Other investigators in the field have previously reported that cannabinoid exposure during pregnancy (in both rats and humans) can affect offspring development, including impairment of cognitive function, and increased risk of depression and anxiety.

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ScienceDaily (June 29, 2012) — A new study led by University of Pittsburgh researchers reveals that moderate amounts of alcohol — consumed in a social setting — can enhance positive emotions and social bonding and relieve negative emotions among those drinking.

While it is usually taken for granted that people drink to reduce stress and enhance positive feelings, many studies have shown that alcohol consumption has an opposite effect. In a new paper titled “Alcohol and Group Formation: A Multimodal Investigation of the Effects of Alcohol on Emotion and Social Bonding,” research shows that moderate doses of alcohol have a powerful effect on both male and female social drinkers when they are in a group.

The paper is published online inPsychological Science.

According to the researchers, previous alcohol studies testing the impact of alcohol on emotions involved social drinkers consuming alcohol in isolation rather than in groups.

“Those studies may have failed to create realistic conditions for studying this highly social drug,” said Michael A. Sayette, lead author and professor of psychology in Pitt’s Kenneth P. Dietrich School of Arts and Sciences. “We felt that many of the most significant effects of alcohol would more likely be revealed in an experiment using a social setting.”

Sayette and his colleagues assembled various small groups using 720 male and female participants, a larger sample than in previous alcohol studies. Researchers assessed individual and group interactions using the Facial Action Coding System (FACS) and the Grouptalk model for speech behavior.

They concluded that alcohol stimulates social bonding, increases the amount of time people spend talking to one another, and reduces displays of negative emotions. According to Sayette, the paper introduces into the alcohol literature new measures of facial expression and speech behavior that offer a sensitive and comprehensive assessment of social bonding.

Sayette and eight colleagues took special care in the methods they employed to form the groups. Each participant was randomly assigned to a group of three unacquainted “strangers.” Each group was instructed to drink an alcoholic beverage, a placebo, or a nonalcoholic control beverage. Twenty groups representing each gender composition (three males; one female and two males; two males and one female; and three females) were assigned to the three different beverage scenarios. Group members sat around a circular table and consumed three drinks over a 36-minute time span. Each session was video recorded, and the duration and sequence of the participants’ facial and speech behaviors were systematically coded frame by frame.

Results showed that alcohol not only increased the frequency of “true” smiles, but also enhanced the coordination of these smiles. In other words, alcohol enhanced the likelihood of “golden moments,” with groups provided alcohol being more likely than those offered nonalcoholic beverages to have all three group members smile simultaneously. Participants in alcohol-drinking groups also likely reported greater social bonding than did the nonalcohol-drinking groups and were more likely to have all three members stay involved in the discussion.

“By demonstrating the sensitivity of our group formation paradigm for studying the rewarding effects of alcohol,” said Sayette, “we can begin to ask questions of great interest to alcohol researchers — Why does alcohol make us feel better in group settings? Is there evidence to suggest a particular participant may be vulnerable to developing a problem with alcohol?”

The new research sets the stage for evaluation of potential associations between socioemotional responses to alcohol and individual differences in personality, family history of alcoholism, and genetic vulnerability.

Additional Pitt researchers on the project were Pitt graduate students in psychology Kasey Creswell, John Dimoff, and Catharine Fairbairn and professors of psychology Jeffrey Cohn, John Levine, and Richard Moreland. Other researchers included Bryan Heckman, a graduate student in psychology at the University of South Florida, and Thomas Kirchner, a research investigator at the Schroeder Institute for Tobacco Research and Policy Studies.

The study was funded by a grant from the National Institute on Alcohol Abuse and Alcoholism.

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ScienceDaily (June 27, 2012) — Researchers at Weill Cornell Medical College have developed and successfully tested in mice an innovative vaccine to treat nicotine addiction.

In the journal Science Translational Medicine, the scientists describe how a single dose of their novel vaccine protects mice, over their lifetime, against nicotine addiction. The vaccine is designed to use the animal’s liver as a factory to continuously produce antibodies that gobble up nicotine the moment it enters the bloodstream, preventing the chemical from reaching the brain and even the heart.

“As far as we can see, the best way to treat chronic nicotine addiction from smoking is to have these Pacman-like antibodies on patrol, clearing the blood as needed before nicotine can have any biological effect,” says the study’s lead investigator, Dr. Ronald G. Crystal, chairman and professor of Genetic Medicine at Weill Cornell Medical College.

“Our vaccine allows the body to make its own monoclonal antibodies against nicotine, and in that way, develop a workable immunity,” Dr. Crystal says.

Previously tested nicotine vaccines have failed in clinical trials because they all directly deliver nicotine antibodies, which only last a few weeks and require repeated, expensive injections, Dr. Crystal says. Plus, this kind of impractical, passive vaccine has had inconsistent results, perhaps because the dose needed may be different for each person, especially if they start smoking again, he adds.

“While we have only tested mice to date, we are very hopeful that this kind of vaccine strategy can finally help the millions of smokers who have tried to stop, exhausting all the methods on the market today, but find their nicotine addiction to be strong enough to overcome these current approaches,” he says. Studies show that between 70 and 80 percent of smokers who try to quit light up again within six months, Dr. Crystal adds.

About 20 percent of adult Americans smoke, and while it is the 4,000 chemicals within the burning cigarette that causes the health problems associated with smoking — diseases that lead to one out of every five deaths in the U.S. — it is the nicotine within the tobacco that keeps the smoker hooked.

A New Kind of Vaccine

There are, in general, two kinds of vaccines. One is an active vaccine, like those used to protect humans against polio, the mumps, and so on. This kind of vaccine presents a bit of the foreign substance (a piece of virus, for example) to the immune system, which “sees” it and activates a lifetime immune response against the intruder. Since nicotine is a small molecule, it is not recognized by the immune system and cannot be built into an active vaccine.

The second type of vaccine is a passive vaccine, which delivers readymade antibodies to elicit an immune response. For example, the delivery of monoclonal (identically produced) antibodies that bind on to growth factor proteins on breast cancer cells shut down their activity.

The Weill Cornell research team developed a new, third kind — a genetic vaccine — that they initially tested in mice to treat certain eye diseases and tumor types. The team’s new nicotine vaccine is based on this model.

The researchers took the genetic sequence of an engineered nicotine antibody, created by co-author Dr. Jim D. Janda, of The Scripps Research Institute, and put it into an adeno-associated virus (AAV), a virus engineered to not be harmful. They also included information that directed the vaccine to go to hepatocytes, which are liver cells. The antibody’s genetic sequence then inserts itself into the nucleus of hepatocytes, and these cells start to churn out a steady stream of the antibodies, along with all the other molecules they make.

In mice studies, the vaccine produced high levels of the antibody continuously, which the researchers measured in the blood. They also discovered that little of the nicotine they administered to these mice reached the brain. Researchers tested activity of the experimental mice, treated with both a vaccine and nicotine, and saw that it was not altered; infrared beams in the animals’ cages showed they were just as active as before the vaccine was delivered. In contrast, mice that received nicotine and not treated with the vaccine basically “chilled out” — they relaxed and their blood pressure and heart activity were lowered — signs that the nicotine had reached the brain and cardiovascular system.

The researchers are preparing to test the novel nicotine vaccine in rats and then in primates — steps needed before it can be tested ultimately in humans.

Dr. Crystal says that, if successful, such a vaccine would best be used in smokers who are committed to quitting. “They will know if they start smoking again, they will receive no pleasure from it due to the nicotine vaccine, and that can help them kick the habit,” he says.

He adds that it might be possible, given the complete safety of the vaccine, to use it to preempt nicotine addiction in individuals who have never smoked, in the same way that vaccines are used now to prevent a number of disease-producing infections. “Just as parents decide to give their children an HPV vaccine, they might decide to use a nicotine vaccine. But that is only theoretically an option at this point,” Dr. Crystal says. “We would of course have to weight benefit versus risk, and it would take years of studies to establish such a threshold.”

“Smoking affects a huge number of people worldwide, and there are many people who would like to quit, but need effective help,” he says. “This novel vaccine may offer a much-needed solution.”

The study was funded by the National Institutes of Health, the National Foundation for Cancer Research, and the Malcolm Hewitt Wiener Foundation.

The Cornell Center for Technology Enterprise and Commercialization, on behalf of Cornell University, has filed patent applications on the work described in this study.

Psychology professor Eric Muth and electrical and computer engineering professor Adam Hoover have created the Bite Counter, a measurement device that will make it easier for people to monitor how much they eat. Worn like a watch, the Bite Counter device tracks a pattern of wrist-roll motion to identify when the wearer has taken a bite of food. Think of it as a pedometer for eating.

“At the societal level, current weight-loss and maintenance programs are failing to make a significant impact. Studies have shown that people tend to underestimate what they eat by large margins, mostly because traditional methods rely upon self-observation and reporting,” said Muth. “Our preliminary data suggest that bite count can be used as a proxy for caloric count.”

The advantage of the Bite Counter is that it is automated so that user bias is removed. The device can be used anywhere, such as at restaurants or while working, where people find it difficult to manually track and remember calories.

The device is not based on what happens in a single bite (i.e. exact grams or specific food nutrients), but in how it simplifies long-term monitoring. For commercialization, Bite Counters eventually will be sold as simple consumer electronics alongside such familiar devices as activity monitors, heart-rate monitors, GPS watches and pedometers. A device is available from Bite Technologies now for professional and research use at http://www.icountbites.com.

“The device only requires that the user press a button to turn it on before eating and press the button again after the meal or snack is done. In between, the device automatically counts how many bites have been eaten,” Hoover said.

In laboratory studies, the device has been shown to be more than 90 percent accurate in counting bites, regardless of the user, food, utensil or container, according to Hoover. However, there are few existing data on how bite count relates to calorie count or how a bite-counting device could be used for weight loss. The device will allow for such data to be more easily collected.

With prototypes completed and manufacturing under way, devices are being tested in 20 subjects for one month. The devices will store logs of bite-count activities, which will provide researchers baseline data for developing guidelines for completely new and innovative weight-loss studies.

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ScienceDaily (June 20, 2012) — Genetics play a significant role in determining which patients will suffer the most from the disturbing side effects of opiates, commonly prescribed painkillers for severe to moderate pain, according to a new Stanford University School of Medicine study, which pinpoints nausea, slowed breathing and potential for addiction as heritable traits.

“One of the most hated side effects of these opiates, nausea, is strongly inherited,” said Martin Angst, MD, professor of anesthesia and one of two principal investigators for the new study, which explores individual variations in the response to opiate use. The study was published June 20 in Anesthesiology. Genetics also play a likely role in determining which patients will suffer from itchiness and sedation associated with the use of these powerful medications, which include morphine, methadone and oxycodone.

“The study is a significant step forward in efforts to understand the basis of individual variability in response to opioids and to eventually personalize opioid treatment plans for patients,” said Angst, director of the Stanford Human Pain Research Laboratory. “Our findings strongly encourage the use of downstream molecular genetics to identify patients who are more likely or less likely to benefit from these drugs — to help make decisions on how aggressive you want to be with treatment, how carefully you monitor patients and whether certain patients are suitable candidates for prolonged treatment.”

Treatment with opiates, also known as narcotics, is tricky because of this variability in drug response. Certain patients may require 10 times the amount of these painkillers to get the same level of pain relief as others. In fact, in some patients the occurrence of side effects may prevent the use of opioids for effectively alleviating pain. Side effects such as nausea or sedation can be debilitating to some, while nonexistent for others. Similarly, some patients can take medications for months with little addiction potential, while others are at risk within weeks.

Millions of U.S. patients are prescribed opiates for pain each year. A better understanding of the potential risk of side effects motivated the researchers to explore individual variation in pairs of identical and fraternal twins, Angst said. The study was prompted by past genetic studies in animals that have shown a strong genetic component in the response to opiates.

“We rely heavily on narcotics as the cornerstone medication for the relief of pain,” said Angst. “Yet we don’t know the answers to fundamental questions, such as why some people ‘like’ narcotics more than others — drug liking and disliking could be key in determining addiction potential.”

Researchers recruited 121 twin pairs for the randomized, double-blinded and placebo-controlled study. Pain sensitivity and analgesic response were measured by applying a heat probe and by immersing a hand in ice-cold water, both before and during an infusion of the opiate alfentanil, a short-acting painkiller prescribed by anesthesiologists. The team also compared individual variations in levels of sedation, mental acuity, respiratory depression, nausea, itch, and drug-liking/disliking — a surrogate measure of addiction potential — between identical twins, non-identical twins and non-related subjects. This provided an estimate of the extent to which variations in responses to opiates are inherited. For example, the finding that identical twins are more similar in their responses to opiates than non-identical twins suggested inheritance plays a significant role.

Heritability was found to account for 30 percent of the variability for respiratory depression, 59 percent of the variability for nausea and 36 percent for drug disliking. Additionally, up to 38 percent for itchiness, 32 percent for dizziness and 26 percent for drug-liking could be due to heritable factors. An earlier study published by the same researchers in the March issue of Pain reported that genetics accounted for 60 percent of the variability in the effectiveness of opiates in relieving pain.

“Since side effects are common among patients who use opioid medications, it will be beneficial to use such research to help at-risk patients avoid serious, life-threatening complications,” said David Clark, MD, PhD, professor of anesthesia and the other principal investigator for the study.

Other Stanford co-authors included Martha Tingle, RN, research nurse; Laura Lazzeroni, PhD, associate professor of psychiatry and behavioral sciences; Nicholas Phillips, MS, research associate; David Drover, MD, associate professor of anesthesiology; and Amrita Ray, PhD, research scientist. The researchers also collaborated with Gary Swan, PhD, director of the Center for Health Sciences at SRI International in Menlo Park, Calif., who is also a co-author of the study.

The study was supported by a grant from the National Institute on Drug Abuse.

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ScienceDaily (June 18, 2012) — While marijuana use by teens has been increasing since 2005, an analysis of data from 1993 through 2009 by economists at three universities has found no evidence to link the legalization of medical marijuana to increased use of the drug among high school students.

“There is anecdotal evidence that medical marijuana is finding its way into the hands of teenagers, but there’s no statistical evidence that legalization increases the probability of use,” said Daniel I. Rees, a professor of economics at the University of Colorado Denver .

Rees co-authored the study with Benjamin Hansen, assistant professor of economics at the University of Oregon and D. Mark Anderson, assistant professor of economics at Montana State University.

They examined the relationship between the legalization of medical marijuana and marijuana consumption using nationally representative data on high school students from the Youth Risky Behavior Survey (YRBS) for the years 1993 through 2009, a period when 13 states, including Alaska, California, Colorado, Hawaii, Maine, Nevada, Oregon and Washington, legalized medical marijuana. Seventeen states and the District of Columbia now have such laws with legislation pending in seven others.

“This result is important given that the federal government has recently intensified its efforts to close medical marijuana dispensaries,” said Hansen, who studies risky behaviors of adolescents and adults. “In fact, the data often showed a negative relationship between legalization and marijuana use.”

Federal officials, including the Director of the Office of National Drug Control Policy, argue that the legalization of medical marijuana has contributed to the recent increase in marijuana use among teens in the United States and have targeted dispensaries operating within 1,000 feet of schools, parks and playgrounds.

According to the 2011 report “Monitoring the Future National Results on Adolescent Drug Use,” prepared annually by the University of Michigan Institute for Social Research, marijuana use by 10th and 12th graders has risen in the last three years, with roughly one in 15 high school seniors smoking marijuana daily or near-daily. The report, cited in the economists’ study, surveyed 46,700 students in the eighth, 10th and 12th grades, in 400 secondary schools.

The new study “Medical Marijuana Laws and Teen Marijuana Use” currently is a non-peer-reviewed working paper made available by the Institute for the Study of Labor (IZA), a private, non-profit independent research institute based in Bonn, Germany, that conducts internationally oriented labor market research.

Researchers examined the relationship between legalization and a variety of outcomes including: marijuana use at school, whether the respondent was offered drugs on school property, alcohol use, and cocaine use. Their results provided no evidence that legalization led to increases in the use of marijuana at school, the likelihood of being offered drugs on school property, or the use of other substances.

In addition to using the national YRBS, the researchers drew on state YRBS data for the period 1993 through 2009 and data from the National Longitudinal Survey of Youth 1997 (NLSY97). None of these sources provided evidence that teenage marijuana use increases with the legalization of medical marijuana.

The YRBS and NLSY97 contain information on self-reported marijuana use. The researchers also analyzed the Treatment Episode Data Set (TEDS), which contains information on whether patients at federally funded drug treatment facilities tested positive for marijuana upon admission. The results suggested that legalization of medical marijuana was unrelated to the likelihood that patients ages 15-20 tested positive for marijuana.

“We are confident that marijuana use by teenagers does not increase when a state legalizes medical marijuana,” said Montana State’s Anderson, who studies health economics, risky behavior and crime.

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ScienceDaily (June 24, 2012) — Researchers at Yale School of Medicine have zeroed in on a set of neurons in the part of the brain that controls hunger, and found that these neurons are not only associated with overeating, but also linked to non-food associated behaviors, like novelty-seeking and drug addiction.

Published in the June 24 online issue of Nature Neuroscience, the study was led by Marcelo O. Dietrich, postdoctoral associate, and Tamas L. Horvath, the Jean and David W. Wallace Professor of Biomedical Research and chair of comparative medicine at Yale School of Medicine.

In attempts to develop treatments for metabolic disorders such as obesity and diabetes, researchers have paid increasing attention to the brain’s reward circuits located in the midbrain, with the notion that in these patients, food may become a type of “drug of abuse” similar to cocaine. Dietrich notes, however, that this study flips the common wisdom on its head.

“Using genetic approaches, we found that increased appetite for food can actually be associated with decreased interest in novelty as well as in cocaine, and on the other hand, less interest in food can predict increased interest in cocaine,” said Dietrich.

Horvath and his team studied two sets of transgenic mice. In one set, they knocked out a signaling molecule that controls hunger-promoting neurons in the hypothalamus. In the other set, they interfered with the same neurons by eliminating them selectively during development using diphtheria toxin. The mice were given various non-invasive tests that measured how they respond to novelty, and anxiety, and how they react to cocaine.

“We found that animals that have less interest in food are more interested in novelty-seeking behaviors and drugs like cocaine,” said Horvath. “This suggests that there may be individuals with increased drive of the reward circuitry, but who are still lean. This is a complex trait that arises from the activity of the basic feeding circuits during development, which then impacts the adult response to drugs and novelty in the environment.”

Horvath and his team argue that the hypothalamus, which controls vital functions such as body temperature, hunger, thirst fatigue and sleep, is key to the development of higher brain functions. “These hunger-promoting neurons are critically important during development to establish the set point of higher brain functions, and their impaired function may be the underlying cause for altered motivated and cognitive behaviors,” he said.

“There is this contemporary view that obesity is associated with the increased drive of the reward circuitry,” Horvath added. “But here, we provide a contrasting view: that the reward aspect can be very high, but subjects can still be very lean. At the same time, it indicates that a set of people who have no interest in food, might be more prone to drug addiction.”

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ScienceDaily (June 21, 2012) — Cigarette smoking among drug dependent pregnant women is alarmingly high, estimated at 77 to 99%. Programs that treat pregnant patients for substance use disorders often fail to address cigarette smoking despite the clear risks to both mother and child, including ectopic pregnancy, spontaneous abortion, preterm delivery, low birth weight, and Sudden Infant Death Syndrome. However, programs to help people quit smoking do not seem to interfere with drug abuse treatment, and may actually improve drug abstinence rates.

One of the most effective methods of helping people to quit smoking is contingency management, which gives smokers monetary incentives for meeting target goals. Researchers at Johns Hopkins University’s Center for Addiction and Pregnancy recently used contingency management to shape smoking reduction and abstinence in drug-dependent pregnant women, with promising results.

One hundred and three pregnant smokers who were prescribed methadone maintenance for heroin dependence were enrolled in a study comparing three conditions. A third of the women were enrolled in a contingency management shaping program and received escalating monetary incentives for reducing their level of cigarette smoking or by being abstinent as measured by breath carbon monoxide levels. The smoking reduction targets required for monetary incentives increased over time from minimal reduction in the early phases of treatment to the requirement of total abstinence by week 12. A relapse meant no monetary incentive was earned and the participant returned to the lowest level of payment. A third of the women could earn incentives for reduced smoking according to a schedule of payments not connected to the woman’s own smoking behaviour (non-contingent incentives). The final group of women received information about the risks of smoking during pregnancy but received no money for reduced smoking.

All of the groups showed some reduction in smoking levels during the experiment, but the women in the contingency management group greatly outperformed the two other groups. Nearly half of the contingency management women met the target of 75% reduction at least once, and a third of them met criteria for smoking abstinence (100% reduction) at least once by week 12. In contrast, none of the other condition participants met the abstinence criteria and only 2% of participants met the 75% reduction target during the study period.

The benefits of contingency management carried on after the experiment. The women in the contingent group had fewer pre-term births (17%, compared with 25% and 29% in the other two groups) and fewer babies with low birth weight (20%, compared with 38% and 43%), and they reported less smoking in the weeks after birth.

The results of the study indicate that contingency management programs are an effective way to reduce smoking in the hard-to-treat population of drug-dependent pregnant women.

ScienceDaily (June 26, 2012) — While current American Heart Association heart failure prevention guidelines warn against habitual coffee consumption, some studies propose a protective benefit, and still others find no association at all. Amidst this conflicting information, research from Beth Israel Deaconess Medical Center attempts to shift the conversation from a definitive yes or no, to a question of how much.

“Our results did show a possible benefit, but like with so many other things we consume, it really depends on how much coffee you drink,” says lead author Elizabeth Mostofsky, MPH, ScD, a post-doctoral fellow in the cardiovascular epidemiological unit at BIDMC. “And compared with no consumption, the strongest protection we observed was at about four European, or two eight-ounce American, servings of coffee per day.”

The study published June 26 online in the journal Circulation: Heart Failure, found that these moderate coffee drinkers were at 11 percent lower risk of heart failure.

Data was analyzed from five previous studies — four conducted in Sweden, one in Finland — that examined the association between coffee consumption and heart failure. The self-reported data came from 140,220 participants and involved 6,522 heart failure events.

In a summary of the published literature, the authors found a “statistically significant J-shaped relationship” between habitual coffee consumption and heart failure, where protective benefits begin to increase with consumption maxing out at two eight-ounce American servings a day. Protection slowly decreases the more coffee is consumed until at five cups, there is no benefit and at more than five cups a day, there may be potential for harm.

It’s unclear why moderate coffee consumption provides protection from heart failure, but the researchers say part of the answer may lie in the intersection between regular coffee drinking and two of the strongest risk factors for heart failure — diabetes and elevated blood pressure.

“There is a good deal of research showing that drinking coffee lowers the risk for type 2 diabetes, says senior author Murray Mittleman, MD, DrPH, a physician in the Cardiovascular Institute at Beth Israel Deaconess Medical Center, an Associate Professor of Medicine at Harvard Medical School and director of BIDMC’s cardiovascular epidemiological research program. “It stands to reason that if you lower the risk of diabetes, you also lower the risk of heart failure.”

There may also be a blood pressure benefit. Studies have consistently shown that light coffee and caffeine consumption are known to raise blood pressure. “But at that moderate range of consumption, people tend to develop a tolerance where drinking coffee does not pose a risk and may even be protective against elevated blood pressure,” says Mittleman.

This study was not able to assess the strength of the coffee, nor did it look at caffeinated versus non-caffeinated coffee.

“There is clearly more research to be done,” says Mostofsky. “But in the short run, this data may warrant a change to the guidelines to reflect that coffee consumption, in moderation, may provide some protection from heart failure.”

Other study authors are Megan Rice, Sc.D., and Emily Levitan, Sc.D.

The research was supported by grants from the National Institutes of Health.

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ScienceDaily (June 20, 2012) — Thanks to modern science, we know that love lives in the brain, not in the heart. But where in the brain is it — and is it in the same place as sexual desire? A recent international study published in the Journal of Sexual Medicine is the first to draw an exact map of these intimately linked feelings.

“No one has ever put these two together to see the patterns of activation,” says Jim Pfaus, professor of psychology at Concordia University, member of the Center for Studies in Behavioral Neurobiology and a co-author of the study. “We didn’t know what to expect — the two could have ended up being completely separate. It turns out that love and desire activate specific but related areas in the brain.”

Along with colleagues in the U.S. and Switzerland, Pfaus analyzed the results from 20 separate studies that examined brain activity while subjects engaged in tasks such as viewing erotic pictures or looking at photographs of their significant others. By pooling this data, the scientists were able to form a complete map of love and desire in the brain.

They found that that two brain structures in particular, the insula and the striatum, are responsible for tracking the progression from sexual desire to love. The insula is a portion of the cerebral cortex folded deep within an area between the temporal lobe and the frontal lobe, while the striatum is located nearby, inside the forebrain.

Love and sexual desire activate different areas of the striatum. The area activated by sexual desire is usually activated by things that are inherently pleasurable, such as sex or food. The area activated by love is involved in the process of conditioning by which things paired with reward or pleasure are given inherent value. That is, as feelings of sexual desire develop into love, they are processed in a different place in the striatum.

Somewhat surprisingly, this area of the striatum is also the part of the brain that associated with drug addiction. Pfaus explains there is good reason for this. “Love is actually a habit that is formed from sexual desire as desire is rewarded. It works the same way in the brain as when people become addicted to drugs.”

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ScienceDaily (July 9, 2009) — Using a nicotine patch before quitting smoking can double success rates, according to Duke University Medical Center researchers. They say their latest data suggest changes should be made to nicotine patch labeling.

“Right now, the nicotine patch is only recommended for use after the quit date,” explains Jed Rose, director of the Duke Center for Nicotine and Smoking Research and lead author of the paper that is published online in the current issue of the journalNicotine and Tobacco Research.

The current labeling resulted from concerns that using a patch while smoking could lead to nicotine overdose. However, a literature review found concurrent use of a nicotine patch and cigarette smoking appears to be safe.

“People who use the patch before quitting are likely to spontaneously reduce the number of cigarettes they smoke because the patch satisfies their need for nicotine and makes the act of smoking less enjoyable,” he says. It also decreases withdrawal symptoms.

“Yet people are afraid to try a pre-cessation patch because the current labeling recommends users not smoke while on treatment,” Rose says. “That’s why our study is so important. It reinforces the findings of previous studies, which show the value of pre-cessation patch therapy, and demonstrates that using a pre-cessation nicotine patch can make a significant difference in a person’s ability to quit.”

Nearly 25 percent of the population continues to smoke despite the known health risks, according to previously published research. And, up to 90 percent of smokers who receive nicotine replacement therapy relapse within one year.

In an effort to find a successful smoking cessation method, Rose and his colleagues randomized 400 people who smoked an average of slightly more than one pack of cigarettes per day. They were put in four groups who either used a nicotine or placebo patch for two weeks prior to quitting smoking. They were further randomized to smoking their regular brand of cigarettes or a low-tar and nicotine cigarette. Following the quit date, all groups received standard nicotine patch treatment at reduced dosages for a total of 10 weeks.

Twenty-two percent of participants in the pre-cessation nicotine patch groups abstained from smoking continuously for at least 10 weeks, compared to 11 percent in the placebo patch groups.

Although participants who smoked their usual brand fared no better or worse than those who smoked a low-tar cigarette, Rose says switching to a low-tar and nicotine cigarette may circumvent any potential safety or tolerability issues that could occur in some smokers.

Rose also believes similar pre-cessation intervention may work for other drugs used for smoking cessation, but more research is needed to support that hypothesis.

More importantly, Rose says the use of the pre-cessation patch is significant because it helps researchers predict people’s subsequent quit success. “People on the patch are more likely to reduce the number of cigarettes they smoke. We found that is a potent predictor of subsequent abstinence. Smokers who did not reduce their smoking on the patch were less likely to succeed.”

That’s the subject of his new research efforts.

“By monitoring pre-cessation patch smoking levels, we may be able to rescue people who aren’t going to succeed. If the smoker is not spontaneously decreasing the number of cigarettes they are smoking, we may be able to find a different treatment that will work for them rather than letting them stay on an ineffective treatment and fail. ”

This research was supported by a grant from Phillip Morris USA; the company had no role in the planning and execution of the study, data analysis or publication of the results. Jed Rose is one of the inventors of the nicotine patch and received royalties in the past from sales of certain nicotine patches.

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ScienceDaily (Apr. 16, 2012) — Alcoholism can disrupt memory functioning well before incurring the profound amnesia of Korsakoff’s syndrome. For example, associative memory — used in remembering face-name associations — can be impaired in alcoholics. A study of the cognitive and brain mechanisms underlying this deficit, through testing of associative memory performance and processing in study participants during structural magnetic resonance imaging (MRI) scanning, have found that impaired learning abilities are predominantly associated with cerebellar brain volumes.

Results will be published in the July 2012 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

“There are several memory systems and alcoholism does not disrupt all of them,” explained Edith V. Sullivan, a professor in the department of psychiatry and behavioral sciences at Stanford University School of Medicine, and corresponding author for the study. “Chronic alcohol consumption mainly affects episodic memory and working memory.”

Episodic memory is the memory system that ‘files’ personally experienced events associated with a precise spatial and temporal context of encoding, and it appears to have an unlimited capacity. “For example, episodic memory includes memories of vacation such as: ‘when I went to Paris with my husband, I ate a delicious ratatouille for dinner in a very cute restaurant; I can remember the place, how I was dressed, and how I burned my tongue when I tasted the meal,'” said Sullivan, quoting Anne-Lise Pitel, the lead author. “Such memories are unique to the individual. Episodic memory is impaired in some alcoholics, who may have difficulties in remembering a grocery list, a route to a new restaurant, or new face-name associations as encountered in a new job.” Associative memory is a component of episodic memory, she added.

Conversely, working memory is a short-term memory system with a limited capacity, which enables temporary storage and manipulation of information, which is quickly forgotten unless consolidated into a long-term storage system. “Alcoholics have deficits of working memory resulting in difficulties like holding a phone number in mind while dialing it,” Sullivan said.

“This study focused on a cognitive process essential in daily living,” added said Sara Jo Nixon, a professor in the department of psychiatry at the University of Florida. “Effective associative learning and memory processes such as learning that two items ‘go’ together and remembering this link or association later are essential for successful interactions throughout our personal and professional environments. Learning the names of new friends, colleagues or acquaintances is only one example of this type of learning, but it is of particular social and personal importance.”

Sullivan, Pitel, and their colleagues presented learning tasks to two groups: 10 alcoholics (8 men, 2 women) recruited from community treatment centers, outpatient clinics, and hospitals, as well as 10 “controls” or non-alcoholics (5 men, 5 women) recruited from the local community. Tasks were either associative such as face-name, or single-item such as face or name. The participants’ recognition retrieval was designated as “shallow encoding” if the face was recalled as that of a “man,” or “deep encoding” if the face was recalled as “honest.”

“Learning new face-name associations was more difficult than learning new single faces or names whether a control or an alcoholic,” said Sullivan. “Alcoholics had impaired learning abilities for both face-name association and single face or name. Learning performances correlated with different brain regions in alcoholics from those of controls; in particular, associative learning in alcoholics was related to cerebellar brain volumes measured on MRI. This pattern was different from associations we observed in controls, who showed relations between associative learning and limbic system volumes.”

“Mnemonists suggest that our ability to remember face-name associations can be improved if we engage processes such as imagery during learning such as deep processing rather than rely on rote learning or shallow processing,” said Nixon. “These authors asked participants to not only learn the face-name association, but to also judge whether the picture was a man or a woman, which is shallow processing. In another set, while learning the pair, participants were asked to judge whether the person looked ‘honest or not,’ which is deep processing. As Edie notes, alcoholics and controls performed similarly during encoding, requiring more time to complete deep processes vs. shallow processing. Alcoholics, however, were inferior to controls in the accuracy of their memory whether they were asked to recognize the correct face-name pair or simply asked to identify which face they had seen earlier in the task.”

Both Sullivan and Nixon noted that this study helps to underscore the complexities of alcohol’s effects on the brain.

“Even though prompting alcoholics to encode memoranda at a deep level resulted in more specific relations with regional brain volumes than shallow encoding,” said Sullivan, “it did not enable them to take advantage of this strategy and both single-item and associative recognition were impaired.”

“These analyses support and extend previous work suggesting that neurocognitive performance in alcoholics may approach or even match that of controls by utilizing alternative neurobehavioral systems,” added Nixon. “For alcoholics, performance on relatively simple cognitive tasks is positively and widely associated with brain volume; associations not observed in controls. In contrast, brain volumes are associated with performance for controls primarily in more difficult or complex tasks. Furthermore, certain brain areas, such as the cerebellum, appear related to performance only for alcoholics. These differential associations are both provocative and relevant.”

“Impaired memory abilities can have harmful consequences on an alcoholic’s day-to-day functioning,” emphasized Sullivan and Pitel. “At work, alcoholics who have a job with a high cognitive load may have difficulties in learning new tasks. At home, memory disorders may be considered as disinterest in family life and may result in conflicts. Finally, from a clinical perspective, impaired episodic memory in alcoholics may hamper obtaining full benefits from rehabilitation efforts because successful treatment requires: one, learning new knowledge such as the meaning, self-awareness, and consequences of ‘addiction’ or ‘drug;’ and two, to ‘re-experience’ episodes when previously drinking, which enables anticipation and recognition of potentially risky situations.”

The title of the article is “Face-Name Association Learning and Brain Structural Substrates in Alcoholism.”